fibrin and Abscess

Anaerobic bacteria are frequent isolates from the mixed bacterial flora of surgical infections. Recent studies have defined an important role for these microorganisms in determining the overall virulence of these infections. One mechanism underlying this effect is the ability of anaerobes to interact with leukocytes, resulting in impairment of host defense mechanisms. This review will address two such mechanisms. First, short-chain fatty acids generated by Bacteroides species during the stationary phase of culture have been shown to cause global impairment of the microbicidal activity of neutrophils. The observation that inhibition was maximal at low extracellular pH led to the finding that the fatty acids mediated this effect by shuttling protons from the extracellular to cytoplasmic space, thereby causing intracellular acidification with resultant cell dysfunction. Second, local fibrin deposition at the site of infection appears to impair bacterial clearance. Interaction between Bacteroides species and peritoneal macrophages has been shown to induce cell-associated procoagulant activity. This may represent another potential mechanism by which anaerobes impair leukocyte function and predispose to abscess formation.

Topics: Abscess; Animals; Bacteria, Anaerobic; Bacterial Infections; Fibrin; Humans; Hydrogen-Ion Concentration; Leukocytes; Neutrophils; Succinates; Succinic Acid; Surgical Wound Infection

The production of fibrinous exudates plays an important role in determining the outcome of peritoneal infection. Large numbers of bacteria are sequestered within fibrin matrices, thereby retarding bacterial spread throughout the peritoneal cavity and into the bloodstream. This walling-off process is teleologically advantageous in that it lessens early rapid mortality. Recent studies have documented that this same process is probably integral to the development of residual infection in the peritoneum. Bacteria sequestered within fibrin deposits are protected from normal host clearance mechanisms, thereby permitting unopposed proliferation and ultimately the establishment of an abscess. A complete understanding of the cellular and noncellular aspects of the host response to peritoneal infection will suggest novel strategies both to treat and to prevent the development of intraabdominal abscesses and their attendant consequences.

Topics: Abscess; Bacteroides fragilis; Bacteroides Infections; Blood Coagulation Factors; Fibrin; Fibrinolysis; Humans; Peritoneal Cavity; Peritoneal Diseases

Staphylococcus aureus is a frequent cause of skin infection and sepsis in humans. Preclinical vaccine studies with S. aureus have used a mouse model with intraperitoneal challenge and survival determination as a measure for efficacy. To appreciate the selection of protective antigens in this model, we sought to characterize the pathological attributes of S. aureus infection in the peritoneal cavity. Testing C57BL/6J and BALB/c mice, >10(9) CFU of S. aureus Newman were needed to produce a lethal outcome in 90% of animals infected via intraperitoneal injection. Both necropsy and histopathology revealed the presence of intraperitoneal abscesses in the vicinity of inoculation sites. Abscesses were comprised of fibrin as well as collagen deposits and immune cells with staphylococci replicating at the center of these lesions. Animals that succumbed to challenge harbored staphylococci in abscess lesions and in blood. The establishment of lethal infections, but not the development of intraperitoneal abscesses, was dependent on S. aureus expression of alpha-hemolysin (Hla). Active immunization with nontoxigenic Hla(H35L) or passive immunization with neutralizing monoclonal antibodies protected mice against early lethal events associated with intraperitoneal S. aureus infection but did not affect the establishment of abscess lesions. These results characterize a mouse model for the study of intraperitoneal abscess formation by S. aureus, a disease that occurs frequently in humans undergoing continuous ambulatory peritoneal dialysis for end-stage renal disease.

Topics: Abscess; Animals; Antibodies, Neutralizing; Bacterial Toxins; Collagen; Disease Models, Animal; Female; Fibrin; Hemolysin Proteins; Kidney Diseases; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Peritonitis; Staphylococcal Infections; Staphylococcus aureus

The appearance of superior vena cava syndrome secondary to benign disease is rare, and it is extremely rare for this condition to develop as a result of the presence of intraluminal catheters. We report two cases of superior vena cava syndrome secondary to implantation of intracavitary pacemakers. We discuss different types of treatment.

Topics: Abscess; Aged; Catheterization, Central Venous; Catheters, Indwelling; Coronary Angiography; Fibrin; Humans; Male; Middle Aged; Pacemaker, Artificial; Staphylococcus epidermidis; Stents; Superior Vena Cava Syndrome; Vena Cava, Superior; Venous Thrombosis

The "Streptococcus milleri" (SMG) group have been shown to possess factors in vitro that may be involved in pathogenesis. All SMG strains are able to bind fibronectin via a cell-surface protein; the binding ranged from 12 to 198 mol/cell. Strains also bound to platelet-fibrin or fibrin clots and fibrinogen, giving maximum adhesion values of 16.5%, 21.8% and 151 mol/cell respectively. Members of the species S. constellatus produced thrombin-like activity. Lancefield group C SMG aggregated rat platelets, a bacterial cell-surface protein acting as mediator in the reaction. Most of the in-vitro factors did not correlate with each other, an indication that SMG strains possess a wide variety of pathogenic properties that may be involved in the production of abscesses or endocarditis. However, there was a correlation between the binding of large amounts of fibrinogen ( > 100 mol/cell) and the ability to aggregate platelets. This suggests that fibrinogen binding may aid in platelet aggregation.

Topics: Abscess; Animals; Bacterial Adhesion; Blood Platelets; Endocarditis, Bacterial; Fibrin; Fibrinogen; Fibronectins; Platelet Aggregation; Rats; Serotyping; Streptococcal Infections; Streptococcus; Surface Properties

Dermatitis herpetiformis has a characteristic histologic pattern consisting of subepidermal blisters often containing fibrin, infiltrates of neutrophils and nuclear dust at tips of dermal papillae, and papillary dermal edema. These are features of early and evolving lesions. We present two cases of clinically typical dermatitis herpetiformis with previously unreported histologic features that may provide a significant diagnostic clue. In each of these cases there were focal collections of nuclear dust in the cornified layer of the epidermis, a finding that may represent a resolving phase of dermatitis herpetiformis, beyond the usual papillary dermal neutrophilic microabscesses seen in early lesions. Biopsy material was available for immunofluorescent studies in one of the cases presented. In addition to the granular pattern of IgA positivity at the dermal-epidermal junction, which is diagnostic of dermatitis herpetiformis, this biopsy also showed similar IgA positivity in the intracorneal nuclear dust aggregates. In the second case, initial sections showed only intracorneal nuclear dust, but at deeper levels there were more typical diagnostic microabscesses at the tips of dermal papillae.

Topics: Abscess; Adult; Blister; Cell Nucleus; Dermatitis Herpetiformis; Edema; Epidermis; Female; Fibrin; Fibrinogen; Follow-Up Studies; Humans; Immunoglobulin A; Male; Middle Aged; Neutrophils; Skin

Deposition of fibrin within the peritoneal cavity is an integral host response to local infection. To directly assess the role of fibrin deposition in the pathogenesis of intraabdominal abscess formation, the ability to induce abscesses in fibrinogen-depleted mice was examined. We hypothesized that systemic defibrinogenation with ancrod would limit the availability of fibrinogen for deposition within the peritoneal cavity and would therefore impair intraabdominal abscess formation. A gelatin capsule containing 50% sterile feces plus Bacteroides fragilis 1 x 10(9) CFU was inserted IP into control or defibrinogenated mice. System defibrinogenation resulted in alteration of the character of abscess formation, as manifested by reduced abscess size and degree of purulence. Abscesses were significantly smaller (0.18 +/- 0.02 gm [n = 29] vs. 0.09 +/- 0.02 gm [n = 11], p less than 0.01) and less purulent (p less than 0.001) in the ancrod-treated mice than in control animals, despite equal numbers of bacteria in the abscesses recovered from both groups. The effect of ancrod was specific for defibrinogenation, because IP repletion with fibrinogen reversed the ancrod effect on abscess size. In addition to its local effects, systemic fibrinogen depletion resulted in a significant elevation in mortality following IP infection (1 of 30 control animals vs. 10 of 23 ancrod-treated animals, p less than 0.01). However, this was not due to an increase in the magnitude of the B. fragilis bacteremia. These studies demonstrate that fibrin deposition contributes to the pathogenesis of purulent abscess formation and that systemic depletion of fibrinogen may alter host susceptibility to the consequences of infection.

Topics: Abdomen; Abscess; Afibrinogenemia; Ancrod; Animals; Bacteroides fragilis; Bacteroides Infections; Disease Susceptibility; Feces; Female; Fibrin; Male; Mice; Rats; Rats, Inbred Strains

The synergic relationship between Escherichia coli and Bacteroides fragilis was examined in a model of intra-abdominal abscess formation. The addition of B. fragilis to E. coli in the fibrin clot inoculum increased abscess weight and residual numbers of E. coli in the abscess at 7 days. In a reciprocal fashion, E. coli was capable of enhancing B. fragilis persistence in abscesses. Neither heat-killed E. coli nor heat-killed B. fragilis was able to mimic the synergic effect of its live counterpart. Furthermore, B. fragilis culture filtrate was unable to reproduce the ability of live B. fragilis to act synergically with E. coli. For B. fragilis to act synergically with E. coli, it had to be inoculated locally with E. coli in the peritoneal cavity, indicating that an effect on systemic resistance by B. fragilis was an unlikely mechanism for the production of bacterial synergy. These studies suggest that the synergic relationship between bacteria in polymicrobial infections is a complex one, resulting from intimate interactions between bacteria and the host in the local milieu of the infection.

Topics: Abscess; Animals; Bacteroides fragilis; Bacteroides Infections; Disease Models, Animal; Escherichia coli; Escherichia coli Infections; Fibrin; Male; Peritonitis; Rats; Rats, Inbred Strains

Topics: Abscess; Combined Modality Therapy; Debridement; Fibrin; Humans; Middle Aged; Peritoneal Lavage; Peritonitis; Postoperative Complications

We inoculated 120 rats with 2 X 10(9) Escherichia coli or 2 X 10(9) Bacteroides fragilis suspended in normal saline solution or incorporated into fibrin clots. In the control group, all animals died after inoculation with E coli, but none died after the inoculation with B fragilis; both were suspended in normal saline solution. Escherichia coli entrapped in fibrin did not cause mortality but did result in abscess formation in all animals. Bacteroides fragilis incorporated into fibrin clots resulted in abscess formation in the majority of animals. Treatment with gentamicin sulfate, ampicillin sulfate, and cefoxitin sodium completely abolished the mortality secondary to E coli suspended in normal saline solution but did not influence the rate of abscess formation secondary to E coli incorporated into fibrin clots. Similarly, cefoxitin and clindamycin phosphate did not significantly change abscess formation secondary to B fragilis incorporated into fibrin clots. We conclude that systemic antibiotics are ineffective in the prevention of abscesses secondary to bacteria trapped in fibrin, either because they do not reach bactericidal levels in the fibrin clot, as in the case of gentamicin, ampicillin, and clindamycin, or, as in the case of cefoxitin, because of the inoculum effect caused by the high number of bacteria. Fibrinogen or fibrin itself do not afford any protection of bacteria against the action of antibiotics.

Topics: Abscess; Ampicillin; Animals; Anti-Bacterial Agents; Ascites; Bacteroides fragilis; Bacteroides Infections; Blood Coagulation; Cefoxitin; Clindamycin; Escherichia coli; Escherichia coli Infections; Fibrin; Gentamicins; Male; Rats; Rats, Inbred Strains

The effect of aprotinin on the clinical and pathologic course of experimentally induced peritonitis in the rat was studied. Peritonitis was induced in 40 rats by creating a closed ileal loop 4 cm long 5 cm from the ileocecal valve. The rats were divided into two groups of 20 rats each. Group 1 served as a control group, whereas each animal in Group 2 received a bolus dose of aprotinin (10 ml) intraperitoneally immediately after closing the laparotomy. In the aprotinin-treated group, survival was drastically increased (p less than 0.01) and formation of adhesions and abscesses was considerably reduced. The results of peritoneal cultures showed a decreased incidence of Escherichia coli and Clostridia in the aprotinin-treated group. We conclude that the administration of aprotinin significantly prolongs the survival time of animals with peritonitis and reduces the development of adhesions and abscesses in the peritoneal cavity. This beneficial effect can be attributed to decreased fibrinogen deposits within the peritoneal cavity and the stabilization of the organism after bacterial shock. Thus, bacteria were more susceptible to cellular and noncellular clearing mechanisms.

Topics: Abscess; Animals; Aprotinin; Clostridium Infections; Escherichia coli Infections; Female; Fibrin; Male; Peritonitis; Rats; Rats, Inbred Strains; Surgical Wound Infection; Tissue Adhesions

We have reviewed 74 cases of patients with permanent pacing, using different types of pacing leads in order to determine what morphological changes are produced by this therapy. Macroscopic examination of the heart was performed and slides at the implantation site reviewed when available. Severe chronic inflammation, scarring and a myocardial response were the prominent findings. From a strictly morphological aspect, the initial trauma at implantation time, the chronic foreign body reaction and myocardial response to chronic trauma, are both much less significant in endovenous than in epimyocardial pacing.

Topics: Abscess; Aged; Autopsy; Cardiomyopathies; Female; Fibrin; Humans; Male; Middle Aged; Myocardium; Necrosis; Pacemaker, Artificial

We measured the rate of lethality and abscess formation in rats that underwent intraperitoneal implantation of fibrin clots contaminated with either Escherichia coli or Bacteroides fragilis alone or in combination, to determine whether the two organisms together would produce a synergistic infection. Ten-day mortality produced by 10(9) colony-forming units (CFU) of E coli was 33.3%. Encapsulated B fragilis led to 3.3% mortality. Escherichia coli (5 X 10(8) CFU) plus B fragilis (5 X 10(8) CFU) led to a sharp increase both in the rate and final ten-day mortality (80.0%). Eighty percent of the rats that received E coli (10(9) CFU within fibrin clots) had abscesses determined on the basis of grossly purulent material. All animals that received B fragilis and survived ten days contained abscesses. Synergy between E coli and B fragilis was noted to occur only when 5 X 10(8) CFU of each organism was present within the fibrin clot. Lower numbers did not produce significant synergy compared with controls that received either E coli or B fragilis. Quantitation of the number of organisms present at 24 hours within contaminated fibrin clots demonstrated a similar amount of growth of both organisms, either when added alone or in combination as copathogens.

Topics: Abscess; Animals; Bacteroides fragilis; Bacteroides Infections; Blood; Blood Coagulation; Disease Models, Animal; Escherichia coli; Escherichia coli Infections; Fibrin; Humans; Peritoneal Cavity; Peritonitis; Rats

Sixty Sprague-Dawley rats were inoculated with 10(9) Escherichia coli either suspended in 2 milliliters of normal saline solution or incorporated in a 2 milliliter 0.4 per cent fibrin clot. One hour after inoculation, one-half of the rats in each group received gentamicin, 12.5 milligrams per kilogram, intramuscularly. Escherichia coli suspended in normal saline solution was uniformly lethal. Incorporation of the bacteria and fibrin resulted in a survival of 13 of 15 rats (p = less than 0.002), but in abscess formation in all survivors. Treatment with gentamicin nearly abolished the mortality of Escherichia coli suspended in normal saline solution (14 of 15 rats survived, p = less than 0.002) but did not prevent abscess formation when bacteria were incorporated into fibrin. The gentamicin level exceeded the minimal inhibitory concentration (0.98 microgram per milliliter) for the strain of Escherichia coli used in serum (15.84 micrograms per milliliter after one hour) and peritoneal fluid (14.75 micrograms per milliliter after one hour) but never reached inhibitory levels in the fibrin clot (0.75 microgram per milliliter after one hour). We conclude that entrapment of bacteria by fibrin abolishes systemic sepsis but also protects bacteria against the action of systemic antibiotics and favors abscess formation.

Topics: Abscess; Animals; Drug Resistance, Microbial; Escherichia coli; Fibrin; Gentamicins; Male; Peritonitis; Rats; Rats, Inbred Strains

The effect of heparin upon the clinical and pathologic course of experimentally induced peritonitis in the rat was studied. Peritonitis was induced in 40 rats by creating a closed ileal loop 4 centimeters long at a distance of 5 centimeters from the ileocecal valve. The rats were divided into two groups of 20 each. The first group served as the control group while each rat of the second group received 30 units of heparin subcutaneously per day postoperatively. Survival was drastically increased in the group receiving heparin (p = 0.001). Adhesion or abscess formation was considerably reduced in this group. The results of peritoneal cultures showed decreased incidence of Escherichia coli and clostridia in the heparin-treated group. Blood cultures also showed decreased incidence of both aerobes and anaerobes in the treated group. It is concluded from this that the administration of heparin significantly prolongs survival time of animals with peritonitis and reduces the development of adhesions and abscesses in the peritoneal cavity. This beneficial effect could be attributed to decreased fibrinogen deposits within the peritoneal cavity, thus rendering the bacteria more susceptible to cellular and noncellular clearing mechanisms.

Topics: Abscess; Animals; Bacterial Infections; Clostridium; Escherichia coli; Female; Fibrin; Heparin; Male; Peritoneal Cavity; Peritonitis; Rats; Rats, Inbred Strains; Tissue Adhesions

Experimental infection in mice with Dermatophilus (D.) congolensis-like microorganisms was carried out, intraperitoneally and subcutaneously. This strain had been isolated from porcine tonsil and reported to be different in some morphological and biological points from D. congolensis. Macroscopic examination revealed multiple abscesses in the peritoneal cavities, or subcutaneous abscesses after the intraperitoneal or subcutaneous injection respectively. Histopathologic examination revealed the characteristic arrangement of the neutrophils surrounding the bacterial colony and peripheral macrophages in the abscess lesions. The lesions contained many microorganisms which showed wide range of the characteristic morphologic variation such as: mycelial elements, coccoid elements and large coccoid elements with transverse or longitudinal septa. Chlamydospore-like elements were sometimes found in the microcolonies in early lesions. The morphology of the lesions and the microorganisms was compared with those of other bacteria including D. congolensis.

Topics: Abscess; Actinomycetales; Actinomycetales Infections; Animals; Fibrin; Granuloma; Inflammation; Liver Abscess; Macrophages; Mice; Necrosis; Neutrophils; Palatine Tonsil; Pancreatic Diseases; Peritoneal Cavity; Splenic Diseases; Swine

We have previously shown that fibrin can act to contain microorganisms and prevent early septic death in experimental peritonitis. However, this trapping eventuates in abscess formation. Fibrinogen, the precursor molecule of fibrin, is known to possess binding structures for some pathogenic organisms. We compared the extent of incorporation of various aerobic and anaerobic bacteria as well as polystyrene latex microspheres into fibrin clots. Similar numbers of organisms and microspheres were incorporated into either noncontracted or contracted fibrin clots. Detailed comparisons of the binding of Escherichia coli or Staphylococcus aureus to human fibrinogen were then made. The addition of 111:B4 lipopolysaccharide did not inhibit incorporation of E. coli 0111:B4 into either type of fibrin clot. With initial inoculum sizes of 10(6) to 10(8) colony-forming units (CFU)/ml, S. aureus was better incorporated into contracted fibrin clots (P less than 0.01) than was E. coli, possible evidence for an easily saturable receptor mechanism. We concluded that microorganisms are incorporated into the polymerizing fibrin matrix in the same fashion as are inert particles of similar size, irrespective of external chemical structure. Adherence of bacteria to fibrinogen or polymerizing fibrin did not appear to represent a specific bacterial virulence factor, more likely representing an effective host defense mechanism of broad specificity.

Topics: Abscess; Animals; Bacteria; Blood Bactericidal Activity; Blood Coagulation; Escherichia coli; Fibrin; Fibrinogen; Lipopolysaccharides; Microspheres; Peritonitis; Polymers; Staphylococcus aureus

Fibrin has classically been considered a defense mechanism of the peritoneal cavity. We have studied the role of purified fibrin in the pathogenesis of intraperitoneal infection. Implantation of 0.5% bovine fibrin clots containing 2 X 10(8) E. coli into the rat peritoneal cavity reduces the 24-hour mortality rate from 100% to 0% compared to bacteria in a similar volume of saline solution. However, the 10-day mortality rate with fibrin is 90%; 100% develop intraperitoneal abscesses. Animals receiving sterile clots lyse than over 1 to 2 weeks without abscess formation. As few as 10(2) E. coli per fibrin clot produce abscesses, but 10(7) or more are required to produce death; without fibrin less than 10(7) E. coli neither kill nor produce intraperitoneal infections. Both late death and abscess size with 2 X 10(8) E. coli are directly proportional to the fibrin clot size but not the concentration of fibrin in the clot. Operative debridement of the fibrin at 4 or 24 hours completely eliminates abscess formation in surviving animals. In vitro growth of E. coli is neither stimulated nor inhibited by fibrin or fibrinogen. Fibrin delays systemic sepsis, but the entrapped bacteria cannot be easily eliminated by normal intraperitoneal bactericidal mechanisms and abscess formation occurs. Thus radical peritoneal debridement or anticoagulation may reduce the septic complications of peritonitis.

Topics: Abscess; Animals; Escherichia coli; Escherichia coli Infections; Fibrin; Fibrinogen; Fibrinolysis; Male; Peritoneal Cavity; Peritonitis; Rats; Time Factors

Topics: Abscess; Ampicillin; Animals; Blood Coagulation; Fibrin; Humans; In Vitro Techniques; Oxacillin; Pasteurella; Protein Binding; Rabbits; Wound Infection

Infection is well recognized as a complication of intrauterine transfusion. The majority of cases are fortunately mild and consist merely of chorio-amnionitis. The present case, of severe type, resulted from contamination of the donor blood with Acinetobacter calcoaceticus. Spread of infection from foetus to mother has been carefully studied and an entirely new type of lesion in the placenta described. This takes the form of acute villous inflammation with resultant micro-abscess formation beneath the trophoblast layer and eventual rupture into the intervillous space. Attempts at localization are poor.

Topics: Abscess; Alcaligenes; Bacterial Infections; Blood Transfusion, Intrauterine; Coombs Test; Female; Fetal Diseases; Fibrin; Humans; Inflammation; Male; Myocardium; Placenta Diseases; Pregnancy; Pregnancy Complications; Trophoblasts

Topics: Abscess; Fibrin; Humans; Lung; Lung Abscess; Lung Neoplasms; Neoplasms